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1.
Asian Journal of Andrology ; (6): 356-360, 2023.
Artigo em Inglês | WPRIM (Pacífico Ocidental) | ID: wpr-981950

RESUMO

Enhanced recovery after surgery (ERAS) measures have not been systematically applied in transurethral surgery for benign prostatic hyperplasia (BPH). This study was performed on patients with BPH who required surgical intervention. From July 2019 to June 2020, the ERAS program was applied to 248 patients, and the conventional program was applied to 238 patients. After 1 year of follow-up, the differences between the ERAS group and the conventional group were evaluated. The ERAS group had a shorter time of urinary catheterization compared with the conventional group (mean ± standard deviation [s.d.]: 1.0 ± 0.4 days vs 2.7 ± 0.8 days, P < 0.01), and the pain (mean ± s.d.) was significantly reduced through postoperative hospitalization days (PODs) 0-2 (POD 0: 1.7 ± 0.8 vs 2.4 ± 1.0, P < 0.01; POD 1: 1.6 ± 0.9 vs 3.5 ± 1.3, P < 0.01; POD 2: 1.2 ± 0.7 vs 3.0 ± 1.3, P < 0.01). No statistically significant difference was found in the rate of postoperative complications, such as postoperative bleeding (P = 0.79), urinary retention (P = 0.40), fever (P = 0.55), and readmission (P = 0.71). The hospitalization cost of the ERAS group was similar to that of the conventional group (mean ± s.d.: 16 927.8 ± 5808.1 Chinese Yuan [CNY] vs 17 044.1 ± 5830.7 CNY, P =0.85). The International Prostate Symptom Scores (IPSS) and quality of life (QoL) scores in the two groups were also similar when compared at 1 month, 3 months, 6 months, and 12 months after discharge. The ERAS program we conducted was safe, repeatable, and efficient. In conclusion, patients undergoing the ERAS program experienced less postoperative stress than those undergoing the conventional program.


Assuntos
Masculino , Humanos , Hiperplasia Prostática/complicações , Qualidade de Vida , Ressecção Transuretral da Próstata/efeitos adversos , Resultado do Tratamento , Recuperação Pós-Cirúrgica Melhorada
2.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-773771

RESUMO

OBJECTIVE@#To investigate the effect of Yiqi Wenyang Huoxue Huatan Fang (YWHHF) on alleviating hypoxia-hypercarbia pulmonary hypertension by inhibiting endothelial-mesenchymal transition (EndoMT) BMP-7/Smads pathway.@*METHODS@#Fifty male healthy SD rats of clean grede, weighting (180~220) g, were randomly divided into 5 groups (=10):normoxia group (N), hypoxia-hypercarbia group (HH); YWHHF high dose group (YH), middle dose group (YM) and low dose group (YL). The rats in N group were kept in normal oxygen environment, the remaining four groups were intermittently exposed to hypoxia-hypercarbia environment (9%~11% O, 5%~6% CO) for 4 weeks, 6 days a week, 8 hours per day. The rats in YH, YM, YL groups were received YWHHF gavage in a dosageof 0.6, 0.3, 0.15g/kg respectively (3 ml/kg),the rats in N and HH groups were received equal volume of normal saline. After 4 weeks, the mean pulmonary arterial pressure(mPAP) was detected,the right ventricular free wall and left ventricle plus ventricular septum were isolated to determine the right ventricular hypertrophy index. Lung ultrastructural changes were surveyed under an electronic microscopy, the changes of pulmonary artery structure surveyed by immunofluorescence, the mRNA levels of alpha-smooth muscle actin (α-SMA)、platelet endothelial cell adhesion molecule-1 (CD31)、bone morphogenetic protein-7 (BMP-7)、drosophila mothers against decapentaplegic protein1/5/8 (Smad1/5/8) were detected by RT-PCR, and the protein levels of α-SMA、CD31、BMP-7、p-Smad1/5/8 and Smad1/5/8 were detected by Western blot.@*RESULTS@#Compared with N group, mPAP and the right ventricular hypertrophy index were increased,some significant injuries also were discovered under microscopic observation,the mRNA and protein expression of α-SMA was increased, and the mRNA expressions of CD31、BMP-7、Smad1/5/8 were decreased in the other four groups, the protein expressions of CD31、BMP-7、p-Smad1/5/8 were decreased(<0.05). Compared with HH group, the above changes in YH、YM、YL groups were all improved (<0.05).@*CONCLUSIONS@#YWHHF can inhibit EndoMT to alleviate pulmonary hypertension, and the mechanism may be related to the promotion of the expression of BMP-7/Smads pathway.


Assuntos
Animais , Masculino , Ratos , Hipercapnia , Hipertensão Pulmonar , Hipóxia , Artéria Pulmonar , Ratos Sprague-Dawley
3.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-773750

RESUMO

OBJECTIVE@#To observe the pulmonary vascular remodeling in rats with pulmonary hypertension induced by hypoxia and hypercapnia, and to explore the role of endoplasmic reticulum stress in pulmonary hypertension.@*METHODS@#Forty SD rats were random-ly divided into four groups:normoxic control group (N), hypoxia hypercapnia group (HH), ERS inhibitor 4-phenylbutyric acid group (4-PBA), endoplasmic reticulum stress (ERS) pathway agonist tunicamycin group (TM), ten rats in each group.The mean pulmona-ry artery pressure (mPAP), mean carotid artery pressure (mCAP) and right ventricular hypertrophy index of rats in each group were measured.Pulmonary artery smooth muscle cells were identified by immunofluorescence α-smooth muscle actin (α-SMA).Morphologi-cal changes of lung tissue and pulmonary artery were observed by electron microscope.The apoptotic index of pulmonary artery smooth muscle cells in each group was detected by TUNEL.Reverse transcription polymerase chain reaction (RT-PCR) and Western blot were used to detect the expression of glucose-regulated protein (GRP78), C/EBP homologous protein (CHOP), c-Jun N-terminal kinase (JNK) and cysteinyl aspartate specific proteinase-12 (caspase-12) mRNA and protein in each group.@*RESULTS@#①Compared with the N group, the mPAP, the ratio of right ventricle weight to left ventricle plus ventricular septum weight[RV/(LV+S)]and the ratio of pulmonary artery wall area to total tube area (WA/TA) were increased (<0.01), and the ratio of pulmonary artery luminal area to total tube area (LA/TA) were decreased (<0.01), pulmonary artery smooth muscle cell apoptosis index were decreased (<0.05 or <0.01) in HH group, 4-PBA group and TM group.ERS related protein and mRNA expressions were increased, the differences were statistically significant.②Compared with the HH group, the mPAP, [RV/(LV+S)]and WA/TA of 4-PBA group were decreased ( <0.01), LA/TA and pulmonary artery smooth muscle cell apoptosis index were increased (<0.01, <0.05).The expressions of ERS related protein and mRNA were all decreased (<0.05 or <0.01).③Compared with the HH group, the mPAP, [RV/(LV+S)]and WA/TA of TM group were increased (<0.05 or <0.01), pulmonary artery middle layer thickened, LA/TA and pulmonary artery smooth muscle cell apoptotic index were decreased (<0.01).ERS related protein and mRNA expressions were increased with statistical significance except GRP78 protein.@*CONCLUSIONS@#Pulmonary vascular remodeling in rats with pulmonary hypertension induced by hypoxia and hypercapnia may be related to the excessive proliferation of pulmonary artery smooth muscle cells and too little apopto-sis;ERS related factors (JNK, caspase-12 and CHOP) are involved in the regulation of pulmonary hypertension induced by hypoxia hypercapnia.


Assuntos
Animais , Ratos , Estresse do Retículo Endoplasmático , Hipercapnia , Hipertensão Pulmonar , Hipóxia , Artéria Pulmonar , Ratos Sprague-Dawley
4.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-696177

RESUMO

Objective To detect the level of CD4+CD25+FoxP3+ (Treg) and Th1,Th2 cells in peripheral blood of patients with immune thrombocytopenia and discuss its clinical significance.Methods Flow cytometry was used to detect the percentage of Treg cells and Th1,Th2 cells in peripheral blood of 27 patients with ITP.25 healthy volunteers were detected as control group.Results The percentage of Treg cells in the peripheral blood of patients with ITP was (2.20 ± 0.93)%,which significantly decreased compared with the healthy control group (2.99 ± 0.45) % (t =3.820,P<0.01) respectively,and the levels of Th1,Th2 cells were not statistically different between the two groups (tTh1 =0.655,tTh2 =0.467,all P> 0.05).Conclusion Treg cells in patients with ITP were decreased,and its important role in the development of ITP deserves further study.

5.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-334005

RESUMO

The aim of this study was to investigate the activation ability of CpG oligodeoxynucleotide (CpG ODN) 2216 on the peripheral blood mononuclear cells (PBMNCs) from leukemia patients in remission and the killing effect of activated PBMNCs on K562 cells. PBMNCs obtained from leukemia patients in remission were incubated with CpG ODN 2216. In control group, PBMNCs were incubated with normal saline (NS). The concentrations of cytokines (IFN-gamma, interleukin-12, interleukin-4, interleukin-10) in culture supernatant of PBMNCs from leukemia patients in remission were analyzed by using ELISA kits. The percentages of Th1, Tc1, Th2, Tc2 cells and killed K562 cells were detected by flow cytometry. The results showed that as compared with control group, CpG ODN 2216 induced higher concentrations production of IFN-gamma, IL-12 in supernatant (p < 0.01). There were no differences in IL-4, IL-10 in supernatant as compared with control group (p > 0.05). The percentages of Th1 and Tc1 cells increased significantly after culture with CpG ODN 2216 as compared with control group (p < 0.05). There was no difference between the percentages of Th2 and Tc2 cells in stimulated group and control group. The killing effect of PBMNCs on K562 cells was significantly different between the stimulated group and control group (p < 0.05). It is concluded that CpG ODNs 2216 can induce strong Th1-like immune activation, with the secretion of type-I cytokine and activation of strong CD8(+) T-cell responses. PBMNCs activated by CpG ODNs can more strongly kill k562 cells in vitro.


Assuntos
Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Adulto Jovem , Linfócitos T CD8-Positivos , Alergia e Imunologia , Citometria de Fluxo , Interferon gama , Sangue , Interleucina-12 , Sangue , Interleucina-4 , Sangue , Células K562 , Leucemia , Alergia e Imunologia , Leucócitos Mononucleares , Biologia Celular , Alergia e Imunologia , Ativação Linfocitária , Oligodesoxirribonucleotídeos , Farmacologia , Células Th1 , Alergia e Imunologia , Células Th2 , Alergia e Imunologia
6.
Journal of Experimental Hematology ; (6): 1443-1447, 2009.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-328624

RESUMO

This study was aimed to investigate the apoptosis-inducing effect of gambogic acid (GA) on K562 cell line and its mechanism. The K562 cells were treated with GA at different concentrations and times, the inhibition rates were detected by MTT assay. Apoptosis induced by GA was assayed by Annexin-V/PI doubling staining. The influence of GA on cell cycle was studied by propidium iodide method. The mitochondrial membrane potential was measured by JC assay. The levels of caspase 3, caspase 8 and caspase 9 activated by fluorescein in living K562 cells were measured by caspGLOW(TM) fluorescein staining kit. The results showed that after incubation with GA, K562 cell proliferation was dramatically inhibited in concentration- and time-dependent manners. K562/A02 cells need higher GA concentration (> 2 microg/ml) to show antiproliferative effect, compared with that of K562 cells (> 0.5 microg/ml). Apoptosis could be induced by GA but the influence on cell cycle was not significant. GA could decrease the mitochondrial membrane potential and increase the activated caspase 3, caspase 8, caspase 9 positive cell levels by 2.19%, -1.95%, 34.01% in 24 hr and 60.4%, 71.3%, 77.7% in 48 hr respectively. It is concluded that the GA can significantly inhibit the proliferation of K562 cells without influence on cell cycles. The GA triggers K562 cell apoptosis through both intrinsic and extrinsic pathways.


Assuntos
Humanos , Apoptose , Caspase 3 , Metabolismo , Caspase 8 , Metabolismo , Caspase 9 , Metabolismo , Ciclo Celular , Proliferação de Células , Células K562 , Potencial da Membrana Mitocondrial , Xantonas , Farmacologia
7.
Journal of Experimental Hematology ; (6): 1021-1025, 2008.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-234308

RESUMO

This study was aimed to investigate the change of expression and activity of protein phosphatases type 2A (PP2A) during the apoptosis of NB4 and MR2 cells induced by Arsenic trioxide (ATO). NB4 and MR2 cells were incubated with Okadaic acid (OKA) (0.5 nmol/L), ATO (0.5 - 2.0 micromol/L), and the combination of OKA and ATO at the same doses as in the single-agent treatment respectively. Then the proliferation of NB4 and MR2 cells was determined by MTT assay, the morphologic changes of cells were evaluated by Wright's staining, the apoptosis rates were detected by flow cytometry. At last, the activities of PP2A were evaluated by the serine/threonine phosphatase assay system, and the levels of PP2A subunits were detected by Western blot analysis. The results showed that ATO inhibited proliferation of NB4 and MR2 cells, and the inhibition rates of ATO on the two cells significantly increased after the addition of OKA. OKA could augment the apoptosis of NB4 and MR2 cells induced by ATO. During the apoptosis of NB4 and MR2 cells, the activity of PP2A decreased with increasing concentration of ATO, and OKA augmented the inhibitory effect of ATO on the activity. The level of PP2A structural subunit (PP2A-A) decreased during ATO-induced apoptosis of NB4 and MR2 cells, that expressions of B and C subunits of PP2A were relatively unaltered. It is concluded that the activity of PP2A decreases with increasing concentration of ATO during the apoptosis of NB4 and MR2 cells, and the decrease of the activity of PP2A maybe is related to the repression of expression of PP2A -A subunit; the inhibition of the activity of PP2A can promote the ATO induced apoptosis of NB4 and MRL cells.


Assuntos
Humanos , Apoptose , Arsenicais , Farmacologia , Linhagem Celular Tumoral , Óxidos , Farmacologia , Proteína Fosfatase 2 , Metabolismo
8.
Chinese Journal of Hematology ; (12): 379-383, 2008.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-240009

RESUMO

<p><b>OBJECTIVE</b>To study the changes in expression and activity of protein phosphatases type 2A (PP2A ) during differentiation of NB4 and NB4-MR2 cells induced by all-trans retinoic acid (ATRA), and evaluate the role of PP2A in MR2 resistance to ATRA.</p><p><b>METHODS</b>ATRA, okadaic acid (OKA) and ATRA + OKA at the same dosage were incubated with NB4 and MR2 cells respectively. Wright's staining and NBT reduction test were employed to evaluate the change in the cells. The CD11b expression was measured by flow cytometry. The activity of PP2A was evaluated by serine/threonine phosphatase assay system, and the level of PP2A subunits was detected by Western blot.</p><p><b>RESULTS</b>1) Wright's staining, NBT reduction test and flow cytometry results showed OKA could augment the differentiation of NB4 induced by ATRA, and OKA + ATRA induced slight differentiation of MR2 cells. 2) Phosphatase assay showed a decrease in PP2A phosphatase activity [(534 +/- 43) pmol x min(-1) x microg protein(-1)] in NB4 after ATRA treatment, accompanied with that activity [(959 +/- 83) pmol x min(-1) x microg protein(-1)] in untreated NB4 cells. OKA enhanced the inhibitory effect of ATRA on the activity in NB4. When OKA + ATRA was incubated with MR2, PP2A in the cells was significantly decreased [(229 +/- 23) pmol x min(-1) x microg protein(-1)]. 3) Western blot analysis showed that the level of PP2A catalytic subunit (PP2A/C) was decreased during the course of ATRA-induced NB4 cell differentiation, whereas expressions of every subunits of PP2A in MR2 cells were somewhat unaltered.</p><p><b>CONCLUSION</b>Expression of PP2A/C and activity of PP2A is decreased during differentiation of NB4 induced by ATRA, and no repression of the PP2 activity maybe related to MR2 resistance to ATRA.</p>


Assuntos
Humanos , Diferenciação Celular , Linhagem Celular Tumoral , Leucemia Promielocítica Aguda , Metabolismo , Patologia , Ácido Okadáico , Farmacologia , Fosfoproteínas Fosfatases , Metabolismo , Proteína Fosfatase 2 , Metabolismo , Tretinoína , Farmacologia
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